scholarly journals Novel long noncoding RNA LINC02323 promotes cell growth and migration of ovarian cancer via TGF‐β receptor 1 by miR‐1343‐3p

2020 ◽  
Author(s):  
Yingchun Li ◽  
Zheng Zhao ◽  
Dan Sun ◽  
Yanfei Li
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cell Growth And Migration ◽  
Β Receptor ◽  
And Migration

scholarly journals The Long Noncoding RNA MALAT-1 Is Highly Expressed in Ovarian Cancer and Induces Cell Growth and Migration

PLoS ONE ◽  
2016 ◽  
Vol 11 (5) ◽  
pp. e0155250 ◽  
Author(s):  
Yanqing Zhou ◽  
Xiaying Xu ◽  
Huabing Lv ◽  
Qirong Wen ◽  
Juan Li ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cell Growth And Migration ◽  
And Migration

scholarly journals Long noncoding RNA THAP9-AS1 is induced by Helicobacter pylori and promotes cell growth and migration of gastric cancer

2019 ◽  
Vol Volume 12 ◽  
pp. 6653-6663 ◽  
Author(s):  
Wenxiao Jia ◽  
Jiaqin Zhang ◽  
Fang Ma ◽  
Shengjie Hao ◽  
Xue Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cell Growth ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Cell Growth And Migration ◽  
And Migration

scholarly journals Down-regulated Long Noncoding RNAHOXA11-ASaffects trophoblast cell proliferation and migration by regulatingRND3andHOXA7expression in preeclampsia

2018 ◽  
Author(s):  
Yetao Xu ◽  
Dan Wu ◽  
Jie Liu ◽  
Zhonghua Ma ◽  
Bingqing Hui ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Noncoding Rna ◽  
Trophoblast Cell ◽  
Rna Seq ◽  
Biological Mechanisms ◽  
Aberrant Expression ◽  
Cell Growth And Migration ◽  
And Migration ◽  
Proliferation And Migration

AbstractThe long noncoding RNAHOXA11-ASreveals abnormal expression in numerous human diseases. However, its function and biological mechanisms remain unclear in Preeclampsia (PE). In this study, we report thatHOXA11-ASwas significantly downregulated in preeclampsic placental tissues and could contribute to the occurrence and development of Preeclampsia. Silencing ofHOXA11-ASexpression could significantly suppress trophoblast cell growth and migration, whereasHOXA11-ASoverexpression facilitated cell growth in HTR-8/SVneo, JEG3 and JAR cell lines. RNA-seq analysis also indicated thatHOXA11-ASsilencing preferentially regulated numerous genes associated with cell proliferation and cell migration. Mechanistic analyses showed thatHOXA11-AScould recruit Ezh2 and Lsd1 protein, and regulateRND3mRNA expression in nucleus. In cytoplasm,HOXA11-ASmodulateHOXA7expression by sponged miR-15b-5p, thus affecting trophoblast cell proliferation. Together, these resulting data confirm that aberrant expression ofHOXA11-ASis involved in the occurrence and development of Preeclampsia, and may act as a prospective diagnosis and therapeutic target in PE.

scholarly journals Long Noncoding RNA KCNQ1OT1 Accelerates the Progression of Ovarian Cancer via MicroRNA-212-3/LCN2 Axis

2020 ◽  
Vol 28 (2) ◽  
pp. 135-146 ◽  
Author(s):  
Xiaoqin Lu ◽  
Fuying Wang ◽  
Meizhou Fu ◽  
Yuankun Li ◽  
Lijun Wang
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Migration And Invasion ◽  
Skov3 Cells ◽  
Direct Target ◽  
Rna Interaction ◽  
Cancer Tissues

Long noncoding RNA KCNQ1OT1 (KCNQ1OT1) has been identified to be deregulated in several kinds of cancers. However, its expression pattern and functions in ovarian cancer remain unknown. Bioinformatics analysis showed that miR-212-3p, an identified suppressor in ovarian cancer, was a direct target of KCNQ1OT1, suggesting that KCNQ1OT1 may play a role in ovarian cancer progression via targeting miR-212-3p. Here we aimed to explore the effect of KCNQ1OT1 on the carcinogenesis of ovarian cancer, as well as to investigate miR-212-3p roles in this process. The expression of KCNQ1OT1 and miR-212-3p in ovarian cancer tissues and cells was detected by qPCR. MTT, flow cytometry, wound healing, Transwell chambers, and in vivo tumor formation assays were carried out to assess cell proliferation, apoptosis, migration, invasion, and tumorigenesis, respectively. RNA pulldown and luciferase gene reporter assays were used to evaluate the RNA‐RNA interaction. The results showed that KCNQ1OT1 was overexpressed in ovarian cancer tissues and cells, which closely associated with the advanced clinic process and poor prognosis in ovarian cancer patients. Upregulation of KCNQ1OT1 significantly enhanced cell growth, migration, and invasion and inhibited cell apoptosis via miR-212-3p. In addition, we identified that lipocalin2 (LCN2) was a direct target of miR-212-3p and functioned as an oncogene to promote cell growth and to inhibit cell apoptosis. Furthermore, we observed that KCNQ1OT1 overexpression significantly enhanced the tumorigenesis of SKOV3 cells, whereas this effect was significantly impaired when LCN2 expression was downregulated. Overall, the present study reveals that KCNQ1OT1 functions as an oncogene in ovarian cancer via targeting miR-212-3p/LCN2 axis, which might provide new markers and targets for ovarian cancer diagnosis and treatment.

scholarly journals Androgen Receptor-Activated Enhancers Simultaneously Regulate Oncogene TMPRSS2 and lncRNA PRCAT38 in Prostate Cancer

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 864 ◽  
Author(s):  
Chen ◽  
Song ◽  
Li ◽  
Xie ◽  
Guo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Chromosome 21 ◽  
Cancer Tissue ◽  
Loop Formation ◽  
Enhancer Activity ◽  
Cell Growth And Migration ◽  
And Migration

Prostate cancer is a common carcinoma in males, the development of which involves the androgen receptor (AR) as a key regulator. AR transactivation induces the high expression of androgen-regulated genes, including transmembrane protease serine 2 (TMPRSS2) and long noncoding RNA prostate cancer-associated transcript 38 (PRCAT38). PRCAT38 and TMPRSS2 are both located on chromosome 21, separated by a series of enhancers. PRCAT38 is a prostate-specific long noncoding RNA that is highly expressed in cancer tissue as compared to normal tissue. Here, we show chromatin looping by enhancers E1 and E2 with the promoters for PRCAT38 and TMPRSS2, indicating the co-regulation of PRCAT38 and TMPRSS2 by the same enhancers. The knockout of enhancer E1 or E2 simultaneously impaired the transcription of PRCAT38 and TMPRSS2 and inhibited cell growth and migration. Moreover, the loop formation and enhancer activity were mediated by AR/FOXA1 binding and the activity of acetyltransferase p300. Our findings demonstrate the utilization of shared enhancers in the joint regulation of two oncogenes in prostate cancer cells.

scholarly journals Long Noncoding RNA MIR4697HG Promotes Cell Growth and Metastasis in Human Ovarian Cancer

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Li-qian Zhang ◽  
Su-qing Yang ◽  
Ying Wang ◽  
Qiao Fang ◽  
Xian-jun Chen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Xenograft Model ◽  
Migration And Invasion ◽  
Transcriptional Level ◽  
Skov3 Cells ◽  
Phosphorylated Akt

Ovarian cancer is one of the three most common gynecological malignant tumors worldwide. The prognosis of patients suffering from this malignancy remains poor because of limited therapeutic strategies. Herein, we investigated the role of a long noncoding RNA named MIR4697 host gene (MIR4697HG) in the cell growth and metastasis of ovarian cancer. Results showed that the transcriptional level of MIR4697HG in cancerous tissues increased twofold compared with that in adjacent noncancerous tissues. MIR4697HG was differentially expressed in ovarian cancer cell lines, with the highest levels in OVCAR3 and SKOV3 cells. MIR4697HG knockdown by specific shRNA significantly inhibited cell proliferation and colony formation in both OVCAR3 and SKOC3 cells. Consistently, in a xenograft model of ovarian cancer, MIR4697HG depletion also significantly restricted tumor volumes and weights. Furthermore, MIR4697HG knockdown inhibited cell migration and invasion capacities. Invasion ability was inhibited by 58% in SKOV3 cells and 40% in OVCAR3 cells, and migration ability was inhibited by 73% in SKOV3 cells and 62% in OVCAR3 cells after MIR4697HG knockdown. MIR4697HG knockdown also caused a decrease in matrix metalloprotease-9, phosphorylated ERK, and phosphorylated AKT. These data suggested that MIR4697HG promoted ovarian cancer growth and metastasis. The aggressive role of MIR4697HG in ovarian cancer may be related to the ERK and AKT signaling pathways.

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